About

Huijuan Hu, PhD, is an Associate Professor in the Department of Anesthesiology at Rutgers New Jersey Medical School. Her research focus is not explicitly detailed on the provided page. She is part of the Center for Immunity & Inflammation (CII) and holds the email address hh480@njms.rutgers.edu. Her role involves contributing to the academic and research missions of the department and the center, but specific details about her research background or key contributions are not included in the provided text.

Research topics

• Neuroscience
• Biology
• Medicine
• Cell biology
• Anesthesia
• Chemistry
• Pharmacology
• Internal medicine
• Biochemistry
• Immunology
• Genetics

Selected publications

• Small non-coding RNA profiling in patients with non-muscle invasive bladder cancer

  BMC Cancer · 2025-02-21 · 2 citations

  articleOpen access

  The intricate regulatory roles of small non-coding RNAs (sncRNAs), including PIWI-interacting RNAs (piRNAs) and microRNAs (miRNAs), have been increasingly recognized in the modulation of cellular functions and are associated with the pathogenesis of various diseases, notably cancer. However, the specific dysregulation patterns of sncRNAs in non-muscle-invasive bladder cancer (NMIBC) have yet to be fully delineated, highlighting a significant gap in our current understanding. To elucidate the expressional dynamics of sncRNAs for patients with NMIBC, we characterized the profile of piRNAs and miRNAs by next-generation sequencing. We identified the differentially expressed sncRNAs between tumor and paracancerous tissues and characterized their distribution along the genome. We further revealed a set of immune-related piRNAs and dysregulated miRNAs that might be associated with NMIBC pathogenesis. Differentially expressed piRNAs were predominantly localized at the long arms of chromosomes 13, 1, and 6. Notably, the targets of specific piRNAs, including piR-hsa-2215234, piR-hsa-105306, piR-hsa-102066, and piR-hsa-236465, show significant associated with antigen processing and presentation pathway. Additionally, differentially expressed miRNAs are mainly located on chromosome 14 and their target genes tend to be involved in cancer-related pathways, suggesting their potential regulatory roles in NMIBC. Collectively, this study revealed the global sncRNA dysregulation in NMIBC, and the identified sncRNAs are implicated in the modulation of both immune and cancer pathways, suggesting their contribution to the pathogenesis and potential targets for immunotherapy.

  PublisherOA PDFDOI

• Generation of a homozygous CPAMD8 knockout human embryonic stem cell line (WAe009-A-2R) by CRISPR/Cas9 system

  Stem Cell Research · 2025-02-15

  articleOpen access

  CPAMD8, a constituent of the A2M/C3 (α-2-macroglobulin/complement 3) protein family, is strikingly expressed in the human fetal lens and distal neural retina. Mutations in CPAMD8 have been linked to anterior segment dysgenesis and primary congenital glaucoma. We utilized CRISPR/Cas9 technology to establish a homozygous CPAMD8 knockout human embryonic stem cell line for differentiating retinal organoids, with the intent of exploring the role of CPAMD8 in the early development of the human eye. The CPAMD8 knockout cell line exhibits normal morphology, pluripotency, and karyotype, serving as a valuable research tool for investigating the functions of CPAMD8 in ophthalmology.

  PublisherDOI

• Proneurotrophin-3 contributes to chemotherapy-induced neuropathic pain through TrkC-mediated CCL2 elevation in DRG neurons

  EMBO Reports · 2025-11-26 · 1 citations

  articleOpen access

  Cancer patients undergoing treatment with antineoplastic drugs often experience chemotherapy-induced neuropathic pain (CINP), and therapeutic options for managing CINP are limited. Here, we show that systemic paclitaxel administration upregulates the expression of neurotrophin-3 (Nt3) mRNA and its encoded proneurotrophin-3 (proNT3) protein in the neurons of dorsal root ganglia (DRG), but not in the spinal cord. Blocking this upregulation attenuates paclitaxel-induced mechanical, heat, and cold nociceptive hypersensitivities and spontaneous pain without altering acute pain and locomotor activity in male and female mice. Conversely, mimicking paclitaxel-induced upregulation of DRG proNT3 produces enhanced responses to mechanical, heat, and cold stimuli and spontaneous pain in naive male and female mice. Mechanistically, proNT3 triggers tropomyosin receptor kinase C (TrkC) activation and participates in the paclitaxel-induced increases of C-C chemokine ligand 2 (Ccl2) mRNA and CCL2 protein in the DRG. Given that CCL2 is an endogenous initiator of CINP and that Nt3 mRNA co-expresses with TrkC and Ccl2 mRNAs in DRG neurons, proNT3 likely contributes to CINP through TrkC-mediated activation of the Ccl2 gene in DRG neurons. Thus, proNT3 may be a potential target for CINP treatment.

  PublisherDOI

• STIM1 functionally couples to transient receptor potential ankyrin 1 contributing to nociception

  Pain · 2025-07-16

  articleOpen accessSenior authorCorresponding

  ABSTRACT: STIM1 is a calcium sensor that can sense calcium level changes in the endoplasmic reticulum (ER) and respond to extracellular stimuli. We have reported that STIM1 is expressed in nociceptors. However, its functional significance remains unclear. Here, we show that STIM1 plays an important role in sensing cold, chemical, and noxious mechanical stimuli in both male and female mice. We found that activation of transient receptor potential ankyrin 1 (TRPA1) triggers ER Ca 2+ release, STIM1 translocation, and store-operated Ca 2+ entry (SOCE). Immunostaining and western blot results reveal that TRPA1 is expressed in the ER. In addition, STIM1 deficiency in the primary sensory neurons reduces cold-, allyl isothiocyanate (TRPA1 agonist)-, and bradykinin-induced Ca 2+ entry and nociception. Moreover, intraplantar injection of thapsigargin, an ER Ca 2+ -ATPase inhibitor, evokes nociception and increases pain hypersensitivity, which is significantly attenuated in STIM1 conditional knockout or L3/L4 dorsal root ganglia STIM1 knockdown mice. Mechanistic studies demonstrate that STIM1-mediated SOCE increases neuronal excitability and decreases potassium channel Kv4-mediated outward currents in small to medium-sized dorsal root ganglion neurons, which is abolished by inhibiting the mitogen-activated protein kinase/extracellular receptor kinase pathway. Our findings demonstrate that STIM1 acts as a transducer of nociception and uncover a novel link between STIM1 and TRPA1 ER . Our study also provides new insights into TRPA1-mediated nociception.

  PublisherOA PDFDOI

• Chemical Origin and Transport Limits of Current Multiplication in BiVO4 Photoanodes

  ChemRxiv · 2025-11-25

  article

  Current multiplication, where more than one electron transfer per photon absorbed, has the potential to transform photoelectrochemical solar fuel generation. Yet it remains rarely realized, largely because the underlying chemical pathways enabling this process are poorly understood and key bottlenecks are still unidentified. Here on BiVO4 photoanode, we reveal direct evidence of vanadium-mediated current-multiplication pathway. During glycerol oxidation, reactive intermediates spontaneously inject electrons directly into the BiVO4 conduction band through surface V5+ reduction, thereby enabling single-photon–driven multiple-electron transfer. More importantly, we identify that poor electron transport—independent of classical hole–electron separation—as a critical bottleneck limiting current multiplication. Mo doping significantly enhances electron transport and promotes efficient extraction of the injected electrons, thereby unlocking the current-multiplication potential of BiVO4.

  PublisherDOI

• Withdrawal Note: NT-3 contributes to chemotherapy-induced neuropathic pain through TrkC-mediated CCL2 elevation in DRG neurons

  EMBO Reports · 2025-11-26

  articleOpen access
  PublisherDOI

• Leveraging deep learning to discover interpretable cellular spatial biomarkers for prognostic predictions based on hepatocellular carcinoma histology

  The Journal of Pathology Clinical Research · 2025-06-13

  articleOpen access1st author

  The spatial structure of various cell types in the tumour microenvironment (TME) can provide valuable insights into disease progression. However, identifying the spatial organization of diverse cell types that significantly correlates with patient prognosis remains challenging. In this study, enabled by deep learning-based cell segmentation and recognition, we developed a computational pipeline to systematically quantify the spatial distribution features of tumour cells, stromal cells, and lymphocytes in haematoxylin and eosin (H&E)-stained pathological images of hepatocellular carcinoma (HCC). We identified six cellular spatial features that consistently and significantly correlated with the overall survival of patients in two independent HCC patient cohorts, The Cancer Genome Atlas Program cohort and the Beijing Hospital cohort. Each threshold for patient stratification was the same for both cohorts, and the six features independently served as prognostic indicators when individually analysed alongside clinical variables. Furthermore, the combination of features such as the mean value of cellular diversity around stromal cells (StrDiv-M), the median distance between all cells (CellDis-MED), and the median value of variation coefficient of the distance around stromal cells and their neighbours (CvStrDis-MED) could further stratify the patient prognosis. In addition, incorporating cell spatial features with another clinical feature, microvascular invasion improved prognostic stratification efficacy for patients from both cohorts. In conclusion, by quantifying the cellular spatial organization features in the HCC TME, we discovered novel biomarkers for evaluating tumour prognosis. These findings could promote mechanistic studies of the cellular spatial organization within the HCC TME and potentially guide future clinical treatment.

  PublisherOA PDFDOI

• Lysophosphatidic acid receptor 5 in insular cortex as a potential analgesic target in neuropathic pain

  Neurotherapeutics · 2025-05-20 · 1 citations

  articleOpen access

  Neuropathic pain remains a significant clinical challenge and existing treatments have limited efficacy and often over rely on opioids. Pharmacological inhibition and genetic knockout of lysophosphatidic acid receptor 5 (LPA5) lead to an analgesic effect on nerve injury-induced nociceptive hypersensitivity in rodents. However, the specific pain-associated regions where LPA5 is required for neuropathic pain remain unidentified. Here, we demonstrate a site-specific increase in the levels of Lpa5 mRNA and LPA5 protein in the contralateral insular cortex and hippocampus 3-14 days after chronic constriction injury (CCI) of the unilateral sciatic nerve in mice. Blocking this time-dependent increase through microinjection of adeno-associated virus 5 (AAV5) expressing Lpa5 shRNA (AAV5-LPA5 shRNA) into insular cortex mitigated CCI-induced development of nociceptive hypersensitivities. This effect was not seen after microinjection of AAV5-LPA5 shRNA into the hippocampus. Mimicking this increase through microinjection of AAV5 expressing full-length Lpa5 mRNA into the insular cortex augmented responses to mechanical, heat and cold stimuli and induced ongoing pain in naïve mice. Moreover, systemic administration of selective LPA5 antagonist RLPA-76 alleviated CCI-induced mechanical allodynia and heat hyperalgesia. All treated mice displayed normal locomotor activities. Altogether, these findings suggest that LPA5 in the insular cortex plays a critical role in neuropathic pain genesis and support LPA5 as a potential target for neuropathic pain treatment.

  PublisherDOI

• Chemical reprogramming of fibroblasts into retinal pigment epithelium cells for vision restoration

  Nature Communications · 2025-12-09

  articleOpen access

  Restoring retinal pigment epithelium (RPE) cells is crucial for treating retinal degenerative (RD) diseases, with chemical reprogramming offering a transformative, scalable solution. However, identifying key chemical compounds for generating functional RPE cells from somatic cells remains challenging. Here, we present a two-step chemical reprogramming strategy to convert fibroblasts into functional chemical induced RPE (ciRPE) cells. Leveraging the Single-Cell Reprogramming Compound Finder (scRCF), which integrates transcriptomics-guided predictions with advanced screening, we identified chemical cocktails that precisely reprogram fibroblasts through an intermediate state into ciRPE cells. These ciRPE cells closely mimic the structure and function of native RPE cells, and upon transplantation into RD rats, they seamlessly integrate into host tissue, protect photoreceptors, and restore visual function. Omics and mechanistic analyses revealed that the identified compounds synergistically activate core transcription factors, including Ascl1 and Olig2, orchestrating the reprogramming process. This study provides a scalable, non-integrative approach for generating functional RPE cells, offering a promising strategy for cell replacement therapies targeting RD diseases.

  PublisherDOI

• A0069 – The efficacy and safety of disitamab vedotin (RC48-ADC) combined with immune checkpoint inhibitors in patients with metastatic upper tract urothelial carcinoma: A multicenter real-world study

  European Urology · 2025-03-01

  article
  PublisherDOI

Recent grants

• NIH Grant R01NS087033

  NIH · $1.9M · 2020

• Identification of a Novel DRG-Specific Long Noncoding RNA and its Role in Neuropathic Pain

  NIH · $2.4M · 2021–2027

• NIH Grant R21NS077330

  NIH · $418k · 2014

Frequent coauthors

• Yuan‐Xiang Tao

  Rutgers, The State University of New Jersey

  26 shared

• Lan Lan

  First Affiliated Hospital Zhejiang University

  20 shared

• Alex Bekker

  19 shared

• Yixiao Mei

  19 shared

• Jingsheng Xia

  Drexel University

  17 shared

• Ruby Gao

  Drexel University

  17 shared

• Moutong Chen

  Guangdong Academy of Sciences

  16 shared

• Shi Wu

  16 shared

Labs

• Center for Immunity & Inflammation (CII)PI

  Not provided

Education

• B.S.

  Jiangxi University of Traditional Chinese Medicine

  1984

• M.S.

  China Pharmaceutical University

  1990

• Ph.D.

  China Pharmaceutical University

  1998